New compounds may be able to keep the heart cells of patients who experience a heart attack or stroke intact while also protecting them against additional injury that can happen after such an event.
During a heart attack, the blood supply to the heart is interrupted, starving heart cells and surrounding tissue of oxygen and eventually causing them to die. This drop-off of oxygen--called an ischemic cascade--causes a sudden crush of metabolic waste that damages cell membranes as well as the mitochondria.
Investigators at the Florida campus of the Scripps Research Institute found that inhibiting the enzyme c-jun-N-terminal kinase, or JNK, reduced the total volume of tissue death as much as 34%. It also guarded against further injury from restored blood flow after an attack, a process known as reperfusion, and reduced mitochondrial dysfunction. The study was published Feb. 8 in The Journal of Biological Chemistry.
In previous studies, Scripps researchers found that JNK migrates to the mitochondria during oxidative stress, and coupled with JNK activation, that migration is associated with numerous serious health issues, such as neuronal cell death, stroke and heart attack.
"What we found was that preventing the migration event also protected against the infarction in these animal models," Philip LoGrasso, lead study author and senior scientific director of discovery biology at Scripps Florida, said to FierceBiotechResearch.
LoGrasso said the compounds could also be used to block cell destruction in Parkinson's patients.
Opko Health has licensed the compounds from Scripps, and LoGrasso said the company is getting close to completing toxicology studies.
- read the press release